Abstract
Hypertrophy is a very common pathologic phenomenon of scar hyperplasia after human skin injury and wound healing. In this article, we first proved that naringin could inhibit the proliferation of fibroblasts by MTT experiments. Flow cytometry indicated that naringin could block the cell cycle and promote apoptosis. Transwell experiments showed that naringin could inhibit the motility activity of fibroblasts. We also found that naringin specifically inhibits the kinase activity of Akt and the phosphorylation of Akt in hypertrophic scar fibroblasts by Kinase-Glo, western blot and real-time PCR assays. Subsequently, western blots and real-time PCR indicated that naringin can inhibit phosphorylation of Akt and downstream proteins of Akt. Our data demonstrated that naringin inhibits the development of hypertrophic scars, at least to a certain extent, by its inhibition of Aktp-Ser473/Thr308.
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